CHAPTER 048. ACIDOSIS AND ALKALOSIS (PART 11) PDF

Chapter 048. Acidosis and Alkalosis (Part 11) Alkali Administration Chronic administration of alkali to individuals with normal renal function rarely, if ever, causes alkalosis. However, in patients with coexistent hemodynamic disturbances, alkalosis can develop because the normal cap[r]

Chapter 048. Acidosis and Alkalosis (Part 1) Harrison's Internal Medicine > Chapter 48. Acidosis and Alkalosis Normal Acid-Base Homeostasis Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and rena[r]

Chapter 048. Acidosis and Alkalosis (Part 8) Methanol (See also Chap. e34) The ingestion of methanol (wood alcohol) causes metabolic acidosis, and its metabolites formaldehyde and formic acid cause severe optic nerve and central nervous system damage. Lactic acid, ketoacids, and other uniden[r]

Chapter 048. Acidosis and Alkalosis (Part 14) Chronic respiratory alkalosis is the most common acid-base disturbance in critically ill patients and, when severe, portends a poor prognosis. Many cardiopulmonary disorders manifest respiratory alkalosis in their early to intermediate stages, an[r]

Chapter 048. Acidosis and Alkalosis (Part 13) The clinical features vary according to the severity and duration of the respiratory acidosis, the underlying disease, and whether there is accompanying hypoxemia. A rapid increase in PaCO2 may cause anxiety, dyspnea, confusion, psychosis, and ha[r]

Chapter 048. Acidosis and Alkalosis (Part 12) Metabolic Alkalosis Associated with ECFV Expansion, Hypertension, and Hyperaldosteronism Increased aldosterone levels may be the result of autonomous primary adrenal overproduction or of secondary aldosterone release due to renal overproduction o[r]

Chapter 048. Acidosis and Alkalosis (Part 10) Differential Diagnosis To establish the cause of metabolic alkalosis (Table 48-6), it is necessary to assess the status of the extracellular fluid volume (ECFV), the recumbent and upright blood pressure, the serum [K+], and the renin-aldosterone[r]

Chapter 048. Acidosis and Alkalosis (Part 9) Approach to the Patient: Hyperchloremic Metabolic Acidoses In diarrhea, stools contain a higher [HCO3–] and decomposed HCO3– than plasma so that metabolic acidosis develops along with volume depletion. Instead of an acid urine pH (as anticipated w[r]

Chapter 048. Acidosis and Alkalosis (Part 7) Alcoholic Ketoacidosis: Treatment Extracellular fluid deficits almost always accompany AKA and should be repleted by IV administration of saline and glucose (5% dextrose in 0.9% NaCl). Hypophosphatemia, hypokalemia, and hypomagnesemia may coexist[r]

Chapter 048. Acidosis and Alkalosis (Part 6) Lactic Acidosis An increase in plasma L-lactate may be secondary to poor tissue perfusion (type A)—circulatory insufficiency (shock, cardiac failure), severe anemia, mitochondrial enzyme defects, and inhibitors (carbon monoxide, cyanide)—or to aer[r]

Chapter 048. Acidosis and Alkalosis (Part 5) Metabolic Acidosis Metabolic acidosis can occur because of an increase in endogenous acid production (such as lactate and ketoacids), loss of bicarbonate (as in diarrhea), or accumulation of endogenous acids (as in renal failure). Metabolic acidos[r]

Chapter 048. Acidosis and Alkalosis (Part 4) Approach to the Patient: Acid-Base Disorders A stepwise approach to the diagnosis of acid-base disorders follows (Table 48-3). Care should be taken when measuring blood gases to obtain the arterial blood sample without using excessive heparin. Blo[r]

Chapter 048. Acidosis and Alkalosis (Part 2) Table 48-1 Prediction of Compensatory Responses on Simple Acid-Base Disturbances and Pattern of Changes Range of Values Disorder Prediction of Compensation pH HCO3– PaCO2 Metabolic PaCO2= (1.5 x Low Low Low HCO3-) + 8 ± 2

that their epitopes tend to be cryptic and need reduction to be exposed.In summary, the extent of mucin glycosylation influences both carbohydrate- andpeptide-specific techniques and must be considered in choosing or developing detec-tion strategies. Regardless of the technique selected as most appr[r]

ganic Na2SO4. The use of only inorganic sulfate as a calibrant will give a slightly lowersulfate quantitation than the use of monosaccharide sulfates. Note that it is also necessaryto include a negative control, in which a volume of water is hydrolyzed under the sameconditions, and any reagent sulfa[r]

isolated from the jelly coat from eggs of different species of amphibians (11–15).This chapter gives an overall idea of the strategy of elucidation of primary structureof glycans, the most current nuclear magnetic resonance (NMR) techniques used instructure determination, and some of the mass[r]

shown by treating mucins with proteolytic enzymes and reducing agents that act onthese regions, and noting a resultant decrease in the size of mucin and gel formation(4–6). Intriguingly, more indirect evidence was found when database searches identi-fied a functionally unrelated protein, von Willebr[r]

UK) and 0.25 mg/mL of hyaluronidase (type 1; Sigma, Poole, UK).d. 3T3 Conditioned medium: DMEM is supplemented with 10% FBS, 2 mM glutamine,100 IU/mL of penicillin, 100 µg/mL of streptomycin, and put onto 24-h postconfluent3T3 cell layers for 24 h. After conditioning, the medium is filtered through[r]

4. 3% stacking/4% running gels for SDS-PAGE, electrophoresis apparatus (mini Protean IIsystem; Bio-Rad, Richmond CA), and Laemmli electrophoresis buffers.5. PhosphorImager (Molecular Dynamics, Sunnyvale, CA), with ImageQuant software (or equiv-alent apparatus) to quantify the amount of radioactivity[r]

Note 10)3.3.1.1. INHIBITION OF VESICULAR RER-TO-GOLGI TRANSPORTBY BREFELDIN A (BFA) (SEENOTE 11)1. Treat seven samples of mucin-producing tissue or cells with BFA for 30 min under nor-mal culturing conditions; 10 µg/mL for tissue, 0.1–2 µg/mL for cell lines (see Note 12).2. Metabolically puls[r]